Cited by 116Telomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model OrganismsNeuroinflammation and Neurodegeneration Mechanisms

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Are there roles for brain cell senescence in aging and neurodegenerative disorders?

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Tan, Florence C. C., Hutchison, Emmette R., Eitan, Erez, Mattson, Mark P.·2014·Biogerontology

DOI 10.1007/s10522-014-9532-1PMC PMC4264619

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Abstract

The term cellular senescence was introduced more than five decades ago to describe the state of growth arrest observed in aging cells. Since this initial discovery, the phenotypes associated with cellular senescence have expanded beyond growth arrest to include alterations in cellular metabolism, secreted cytokines, epigenetic regulation and protein expression. Recently, senescence has been shown to play an important role in vivo not only in relation to aging, but also during embryonic development. Thus, cellular senescence serves different purposes and comprises a wide range of distinct phenotypes across multiple cell types. Whether all cell types, including post-mitotic neurons, are capable of entering into a senescent state remains unclear. In this review we examine recent data that suggest that cellular senescence plays a role in brain aging and, notably, may not be limited to glia but also neurons. We suggest that there is a high level of similarity between some of the pathological changes that occur in the brain in Alzheimer's and Parkinson's diseases and those phenotypes observed in cellular senescence, leading us to propose that neurons and glia can exhibit hallmarks of senescence previously documented in peripheral tissues.

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Oxidative Stress: A Key Modulator in Neurodegenerative Diseases
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Cellular senescence in brain aging
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“The concept of neuronal senescence is relatively new even though it is well-established that neuronal functions decline with aging (Tan et al., 2014).”
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Authors: Tan, F. C. C., Hutchison, E. R., Eitan, E., & Mattson, M. P.
Affiliations: National Institute on Aging (US)
Corresponding author: Hutchison, Emmette R.
Eitan, Erez
ORCID: Eitan, Erez
Mattson, Mark P.
Venue: Biogerontology
Publisher: Springer Science and Business Media LLC
Published: 2014-10-11
Volume: 15
Issue: 6
Pages: 643-660
ISSN: 1389-5729 (ISSN-L)
1573-6768
DOI: 10.1007/s10522-014-9532-1
PMC: PMC4264619
OpenAlex: W1977085416
Cited by: 116
References: 191
Citations by year: 2026: 3 · 2025: 6 · 2024: 4 · 2023: 8 · 2022: 14 · 2021: 12 · 2020: 15 · 2019: 16 · 2018: 19 · 2017: 10 · 2016: 4 · 2015: 2 · 2014: 2
FWCI: 0.70
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Biogerontology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (Z99 AG999999)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: cellular senescence, brain aging, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease, neuronal senescence, senescence-associated secretory phenotype, epigenetic regulation, postmitotic neurons, embryonic development
MeSH terms: Aged, Aging, Animals, Brain, Humans, Neuroglia, Neurons, Cellular Senescence, Neurodegenerative Diseases, Epigenesis, Genetic, Mice

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Are there roles for brain cell senescence in aging and neurodegenerative disorders?

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